Modulation of the immunological synapse: a key to HIV-1 pathogenesis?

2007 ◽  
Vol 7 (4) ◽  
pp. 310-317 ◽  
Author(s):  
Oliver T. Fackler ◽  
Andres Alcover ◽  
Olivier Schwartz
Keyword(s):  
Viruses ◽  
2010 ◽  
Vol 2 (5) ◽  
pp. 1239-1260 ◽  
Author(s):  
Gaia Vasiliver-Shamis ◽  
Michael Dustin ◽  
Catarina Hioe

2013 ◽  
Vol 4 ◽  
pp. VRT.S11046 ◽  
Author(s):  
Mohit Sehgal ◽  
Zafar K. Khan ◽  
Andrew H. Talal ◽  
Pooja Jain

Persistent infections with human immunodeficiency virus type 1 (HIV-1) and hepatitis C virus (HCV) are a major cause of morbidity and mortality worldwide. As sentinels of our immune system, dendritic cells (DCs) play a central role in initiating and regulating a potent antiviral immune response. Recent advances in our understanding of the role of DCs during HIV-1 and HCV infection have provided crucial insights into the mechanisms employed by these viruses to impair DC functions in order to evade an effective immune response against them. Modulation of the immunological synapse between DC and T-cell, as well as dysregulation of the crosstalk between DCs and natural killer (NK) cells, are emerging as two crucial mechanisms. This review focuses on understanding the interaction of HIV-1 and HCV with DCs not only to understand the immunopathogenesis of chronic HIV-1 and HCV infection, but also to explore the possibilities of DC-based immunotherapeutic approaches against them. Host genetic makeup is known to play major roles in infection outcome and rate of disease progression, as well as response to anti-viral therapy in both HIV-1 and HCV-infected individuals. Therefore, we highlight the genetic variations that can potentially affect DC functions, especially in the setting of chronic viral infection. Altogether, we address if DCs’ potential as critical effectors of antiviral immune response could indeed be utilized to combat chronic infection with HIV-1 and HCV.


2022 ◽  
Vol 12 ◽  
Author(s):  
Marisierra Espinar-Buitrago ◽  
Ma Angeles Muñoz-Fernández

Due to the success of combined antiretroviral therapy (cART) in recent years, the pathological outcome of Human Immunodeficiency Virus type 1 (HIV-1) infection has improved substantially, achieving undetectable viral loads in most cases. Nevertheless, the presence of a viral reservoir formed by latently infected cells results in patients having to maintain treatment for life. In the absence of effective eradication strategies against HIV-1, research efforts are focused on obtaining a cure. One of these approaches is the creation of therapeutic vaccines. In this sense, the most promising one up to now is based on the establishing of the immunological synapse between dendritic cells (DCs) and T lymphocytes (TL). DCs are one of the first cells of the immune system to encounter HIV-1 by acting as antigen presenting cells, bringing about the interaction between innate and adaptive immune responses mediated by TL. Furthermore, TL are the end effector, and their response capacity is essential in the adaptive elimination of cells infected by pathogens. In this review, we summarize the knowledge of the interaction between DCs with TL, as well as the characterization of the specific T-cell response against HIV-1 infection. The use of nanotechnology in the design and improvement of vaccines based on DCs has been researched and presented here with a special emphasis.


2008 ◽  
Vol 389 (10) ◽  
Author(s):  
Claudia Haller ◽  
Oliver T. Fackler

AbstractCell-cell transmission of human immunodeficiency virus type 1 (HIV-1) is considered the most effective mode of viral spread in T-lymphocyte cultures. Evidence has accumulated that HIV-1 assembles polarized synaptic-like structures, referred to as virological synapses, as specialized sites of viral transfer. Interestingly, it was recently also discovered that HIV-1 impairs the formation of the structurally similar immunological synapse, thereby modulating exogenous T-lymphocyte stimulation to yield an optimal activation state for productive HIV-1 infection. The careful dissection of these opposing effects will contribute to our understanding of retroviral spread and cellular signal transduction machineries.


2007 ◽  
Vol 2007 (Spring) ◽  
Author(s):  
Claudia Haller ◽  
Susanne Rauch ◽  
Nico Michel ◽  
Sebastian Hannemann ◽  
Oliver T. Keppler ◽  
...  

2008 ◽  
Vol 82 (19) ◽  
pp. 9445-9457 ◽  
Author(s):  
Gaia Vasiliver-Shamis ◽  
Michael Tuen ◽  
Teresa W. Wu ◽  
Toby Starr ◽  
Thomas O. Cameron ◽  
...  

ABSTRACT Human immunodeficiency virus type 1 (HIV-1)-infected T cells form a virological synapse with noninfected CD4+ T cells in order to efficiently transfer HIV-1 virions from cell to cell. The virological synapse is a specialized cellular junction that is similar in some respects to the immunological synapse involved in T-cell activation and effector functions mediated by the T-cell antigen receptor. The immunological synapse stops T-cell migration to allow a sustained interaction between T-cells and antigen-presenting cells. Here, we have asked whether HIV-1 envelope gp120 presented on a surface to mimic an HIV-1-infected cell also delivers a stop signal and if this is sufficient to induce a virological synapse. We demonstrate that HIV-1 gp120-presenting surfaces arrested the migration of primary activated CD4 T cells that occurs spontaneously in the presence of ICAM-1 and induced the formation of a virological synapse, which was characterized by segregated supramolecular structures with a central cluster of envelope surrounded by a ring of ICAM-1. The virological synapse was formed transiently, with the initiation of migration within 30 min. Thus, HIV-1 gp120-presenting surfaces induce a transient stop signal and supramolecular segregation in noninfected CD4+ T cells.


Traffic ◽  
2005 ◽  
Vol 6 (6) ◽  
pp. 488-501 ◽  
Author(s):  
Eduardo Garcia ◽  
Marjorie Pion ◽  
Annegret Pelchen-Matthews ◽  
Lucy Collinson ◽  
Jean-Francois Arrighi ◽  
...  

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